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At least 847 records · Page 47Linked to original sources
PubMed2003

Diaphragm pacing during prolonged mechanical ventilation of the lungs could prevent from respiratory muscle fatigue.

UNLABELLED: Respiratory muscle fatigue after prolonged mechanical ventilation of the lungs is a common occurrence. This is probably due to disuse atrophy. The standard technique used to overcome this problem is to gradually wean the patient from the respirator over the course of several days or weeks. HYPOTHESIS: based on experience with the rehabilitation of skeletal muscles during long-term immobilisation of the extremities following trauma or surgery and on experience with diaphragm pacing in quadriplegics, intermittent electrical or magenetic stimulation of the diaphragm while the lungs are still being mechanically ventilated may be beneficial. The result of such stimulation would be to preserve the dysfunctioning diaphragm from atrophy. CONSEQUENCES: dependence on the respirator, length of intubation time, risk of complications and length of stay in the ICU would be considerably reduced.

Diaphragm↗
PubMedDate not supplied

Nemaline cardiomyopathy in a young adult: an ultraimmunohistochemical study and review of the literature.

Heart transplantation was performed in a 26-year-old man who suffered from severe dilatative cardiomyopathy. A nemaline myopathy characterized by the accumulation of Z-line material and the formation of rod-like structures had been diagnosed in the skeletal muscle. Routine light microscopy of the heart disclosed only nonspecific findings. On electron microscopy scattered cardiomyocytes showed formations of rod-like structures and a structural desintegration of contractile filaments near the intercalated disks. Immunocytochemistry at the light and electron microscopical level exhibited an accumulation of alpha-actinin, desmin, and occasionally vinculin in abnormal cardiomyocytes. The rods were specifically stained with alpha-actinin and were less immunoreactive for desmin. No mutations were revealed in the skeletal muscle alpha-actin gene. The results illustrate a complex derangement of the cytoskeletal apparatus in nemaline cardiomyopathy. Nemaline cardiomyopathy may be difficult to diagnose in routine diagnostic procedures. A close correlation between the severity of cardiac dysfunction and the morphological expression of the disease in the heart may not be found. Nemaline cardiomyopathy should be included in the differential diagnosis of dilatative cardiomyopathy and may be diagnosed with certainty by ultrastructural-immunhistochemical investigations.

Actinin↗
PubMed2000

The importance of insulin resistance in the pathogenesis of type 2 diabetes mellitus.

Many patients with type 2 diabetes have hyperglycemia as a result of deficiencies in both insulin secretion and insulin action, that is, beta-cell dysfunction and insulin resistance. Insulin resistance is a state of reduced insulin sensitivity, an inability of insulin to lower plasma glucose levels through suppression of hepatic glucose production and stimulation of glucose utilization in skeletal muscle and adipose tissue. Insulin resistance stems from genetic and environmental causes, and its extent varies considerably among individuals. Studies have shown that enhanced insulin secretion can compensate for insulin resistance and that enhanced insulin sensitivity can mask defects in beta-cell function. However, insulin resistance is essential to the development of the majority of cases of type 2 diabetes. Numerous epidemiologic studies have demonstrated an increase in the prevalence of insulin resistance and type 2 diabetes in various ethnic populations that have migrated from their native lands to more urbanized and westernized regions of the world. Type 2 diabetes has already reached epidemic proportions worldwide. By 2025, an estimated 300 million people will have diabetes, most of whom will inhabit China, India, and the United States. These studies have also demonstrated the complex interrelationship of hyperinsulinemia, obesity (primarily visceral adiposity), and free fatty acids with beta-cell dysfunction, insulin resistance, and the development of type 2 diabetes. Although little can be done to avert a genetic predisposition to type 2 diabetes, normoglycemia can be preserved in individuals who remain insulin sensitive. Lifestyle changes can be implemented and medications can be administered to improve insulin sensitivity, insulin secretion, and glucose utilization and reduce the prevalence of type 2 diabetes.

Blood Glucose↗
PubMed1998

Myopathy induced by HMG-CoA reductase inhibitors in rabbits: a pathological, electrophysiological, and biochemical study.

A combination of electrophysiological, pathological, and biochemical studies were performed in myopathy induced by 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors. Simvastatin (a lipophilic inhibitor) or pravastatin (a hydrophilic inhibitor) were administered by gavage to rabbits. In Group I (simvastatin-treated group, 50 mg/kg/day for 4 weeks), four rabbits showed muscle necrosis and high serum creatine kinase (CK) levels, and all six rabbits showed electrical myotonia. In Group II (pravastatin-treated group, 100 mg/kg/day for 4 weeks), no rabbit showed either condition. In Group III (pravastatin-treated group, 200 mg/kg/day for 3 weeks plus 300 mg/kg/day for 3 weeks), one rabbit showed muscle necrosis and high serum CK level and two rabbits showed electrical myotonia. The pathological findings were muscle fiber necrosis and degeneration with increased acid phosphatase activity by light microscopy, autophagic vacuoles and mitochondrial swelling, and disruption and hypercontraction of myofibrils by electron microscopy. Ubiquinone content decreased in skeletal muscle by 22 to 36% in Group I, by 18 to 52% in Group II, and by 49 to 72% in Group III. However, mitochondrial enzyme activities of respiratory chain were normal in all groups. These results indicate that myopathy was not induced by a secondary dysfunction of mitochondrial respiration due to low ubiquinone levels.

Animals↗
PubMed1999

Parvalbumin gene transfer corrects diastolic dysfunction in diseased cardiac myocytes.

Heart failure frequently involves diastolic dysfunction that is characterized by a prolonged relaxation. This prolonged relaxation is typically the result of a decreased rate of intracellular Ca(2+) sequestration. No effective treatment for this decreased Ca(2+) sequestration rate currently exists. As an approach to possibly correct diastolic dysfunction, we hypothesized that expression of the Ca(2+) binding protein parvalbumin in cardiac myocytes would lead to increased rates of Ca(2+) sequestration and mechanical relaxation. Parvalbumin, which is normally absent in cardiac tissue, is known to act as a soluble relaxing factor in fast skeletal muscle fibers by acting as a delayed Ca(2+) sink. As a test of the hypothesis, gene transfer was used to express parvalbumin in isolated adult cardiac myocytes. We report here that expression of parvalbumin dramatically increases the rate of Ca(2+) sequestration and the relaxation rate in normal cardiac myocytes. Importantly, parvalbumin fully restored the relaxation rate in diseased cardiac myocytes isolated from an animal model of human diastolic dysfunction. These findings indicate that parvalbumin gene transfer offers unique potential as a possible direct treatment for diastolic dysfunction in failing hearts.

Animals↗
PubMed2005

Growth factor enhancement of muscle regeneration: a central role of IGF-1.

The prolongation of skeletal muscle strength in aging and neuromuscular disease has been the objective of numerous studies employing a variety of approaches. In the last decade, dramatic progress has been made in elucidating the molecular defects underlying a number of muscle diseases. With the characterization of mutations responsible for muscle dysfunction in several inherited pathologies, and the identification of novel signaling pathways, subtle alterations in which can lead to significant defects in muscle metabolism, the field is poised to devise successful strategies for treatment of this debilitating and often fatal group of human ailments. Yet progress has been slow in therapeutic applications of our newly gained knowledge. The complexity of muscle types, the intimate relationship between structural integrity and mechanical function, and the sensitivity of skeletal muscle to metabolic perturbations have impeded rapid progress in successful clinical intervention. The relatively poor regenerative properties of striated muscle compound also the devastating effects of muscle degeneration.

Animals↗
PubMed2002

Skeletal muscle mitochondrial function and exercise capacity in HIV-infected patients with lipodystrophy and elevated p-lactate levels.

OBJECTIVE: To investigate the skeletal muscle mitochondrial function in HIV-infected patients with lipodystrophy or elevated p-lactate levels. DESIGN: Eight HIV patients treated with highly active antiretroviral therapy, with lipodystrophy or elevated p-lactate, and eight healthy controls were exposed to incremental exercise until exhaustion. METHODS: Blood samples and gas analysis were performed at rest, during exercise and in recovery. Oxygen consumption, workload and blood lactate were assessed. Before and immediately after exercise muscle biopsies were obtained, in which citrate synthase (CS), hydroxyacyl-coenzyme A dehydrogenase (HD), glycogen and nucleotides were measured. RESULTS: Maximal workload was significantly lower in patients compared with controls [171 Watt (88-206) versus 235 Watt (118-294) P = 0.05]. A trend towards lower maximal oxygen consumption (VO(2max)) was detected in patients [2136 ml/min (1221-2598) versus 2985 ml/min (1506-3959) P = 0.11]. Patients had significantly elevated levels of blood lactate at rest [1.55 mmol/l (1-2.5) versus 0.8 mmo/l (0.37-1.1) P < 0.01), but no significant difference in maximal blood-lactate values was found. The decline in blood lactate in the recovery period was similar between groups. There was no significant difference in CS, HD, glycogen or nucleotides. CONCLUSION: The significantly lower working capacity and the trend towards reduced VO(2max) in patients could be caused by mitochondrial dysfunction, but may also be caused by impaired physical fitness. The similar levels of nucleotides, CS, HD, and glycogen and the normal increase in blood lactate during exercise indicates a normal oxidative phosphorylation. No evidence of serious damage to skeletal muscle mitochondrial function was found.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2004

Endothelial dysfunction, inflammation, and insulin resistance: a focus on subjects at risk for type 2 diabetes.

Subjects with obesity, family history of type 2 diabetes, polycystic ovary syndrome, previous gestational diabetes, dyslipidemia, hypertension, impaired glucose tolerance or impaired fasting glucose, and those with metabolic syndrome are at risk for the development of type 2 diabetes. Some of them are also at risk for cardiovascular disease. Some underlying abnormalities such as insulin resistance, endothelial dysfunction, and low-grade chronic inflammation are frequently present and closely associated in all these groups. The flow of substrates, hormones, and cytokines from visceral fat to skeletal muscle and to the endothelial cells, along with some genetic abnormalities that lead to impaired insulin action in the peripheral tissues and to impaired insulin-stimulated nitric oxide production in endothelial cells, may play a role in establishing these shared metabolic and vascular derangements. Weight loss, thiazolidinediones, and metformin improve vascular function in subjects at risk for type 2 diabetes and may prove to reduce cardiovascular events in these individuals.

Animals↗
PubMed1995

Kearns-Sayre syndrome associated with mitochondrial DNA deletion or duplication: a molecular genetic and pathological study.

The neuropathological findings in 2 patients with Kearns-Sayre syndrome and mitochondrial DNA (mtDNA) rearrangements, one a predominant deletion and the other a predominant duplication, were remarkably similar, showing diffuse vacuolation of white matter. There were some of the pathological features of Leigh's syndrome in the spinal cord of the patient with a duplication. In the patient with a predominant deletion, rearranged mtDNA was undetectable in blood, spleen, and testis, and present in highest amounts in muscle and the brain, but relatively low in cerebellum, reflecting the ratio seen, albeit in much smaller amounts, in normal aged brains. MtDNA rearrangements in this patient were largely deletions or deletion dimers; duplicated mtDNA was present in only trace amounts in some tissues and there was none in skeletal muscle. The patient with a predominant duplication of mtDNA had higher amounts of rearranged mtDNA in blood (mainly duplicated) than muscle (mainly deleted). Correlation of these data with tissue dysfunction is probably complicated by the replicative behaviour of deleted, duplicated and normal mtDNA.

Adolescent↗
PubMed1990

[Diagnosis and therapy of myo-arthropathy (Costen's syndrome)].

The temporo-mandibular joint (TMJ) syndrome was first described by Costen in 1936. It is a muscular-skeletal pain-disease. The pain is caused by hypertonia of the masticatory muscles and is projected into various regions of the head and neck. There is a primary dysfunctional etiology as well as a secondary etiology based on other diseases, particularly of the ENT region. Diagnostically, therefore, a process of exclusion is required. The symptoms can range from diffuse headache and facial pain to strictly localized or even neuralgic pain. Otogenic symptoms may be pain or various noises in the ear. For differential diagnosis, most of the painful diseases of the head area must be considered because of the multiform clinical manifestation of the TMJ syndrome. The treatment of the TMJ syndrome follows a multistep scheme that includes behavior therapy, physiotherapeutic methods, and occlusal therapy.

Behavior Therapy↗
PubMed1984

Biomechanics in clinical practice.

Evidence from dynamic biomechanical analyses of physical activities has greatly expanded our knowledge about the mechanical bases for human movement function with potential implications for further understanding movement dysfunction. The purpose of this review is to relate these findings to present knowledge about the effect on human joints during movement, the role of muscle action on human skeletal levers during movement, and the application of this information to functional tasks by physical therapy clinicians. Also presented are some thoughts regarding what must be accomplished so that this material can be generalized to clinical practice.

Ankle Joint↗
PubMed1986

Beta-blockade and carbohydrate metabolism: theoretical aspects and clinical implications.

The adrenergic control of carbohydrate metabolism is expressed at two levels: regulation of substrate flow, and interference with the secretion of hormones. Normally, this adrenergic regulatory system only plays a minor role. However, it is of great importance as an acute adaptation of the body to fight and flight. Under these circumstances, fuel fluxes increase almost instantaneously. Glycogenolysis and gluconeogenesis are responsible for increased hepatic glucose output. Increased fatty acid flux is brought about by stimulated adipose tissue lipolysis, which probably, as a secondary phenomenon, causes decreased peripheral glucose utilisation by the skeletal muscle mass. Cerebral glucose uptake accounts for half the body's basal glucose production. Since this glucose uptake is concentration-dependent only, hypoglycaemia rapidly leads to cerebral dysfunction. To guarantee cerebral glucose uptake, the body has a dual defense mechanism against hypoglycaemia: hormonal and metabolic counteraction. The first consists of the secretion of glucagon and (nor)epinephrine, the latter of hepatic autoregulation and alternative fuels for noncerebral tissues. In clinical practice, the inappropriate insulin-excess state forms the major cause of hypoglycaemia. There is, however, a second reason why patients with diabetes mellitus are at risk. Diabetes by itself leads to impaired glucagon secretion and, when autonomic neuropathy exists, to diminished (nor)epinephrine secretion. Thus, interference with the latter, such as administration of beta-blocking agents, further impairs hypoglycaemic counterregulation. In fact, numerous studies document delayed recovery from experimentally induced hypoglycaemia in diabetic patients receiving beta-blocking agents. However, using beta 1-selective blocking agents, mean recovery from hypoglycaemia in groups of diabetic patients demonstrates minor delay only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1985

Carnitine alterations in spontaneous and drug-induced turkey congestive cardiomyopathy.

Carnitine and acylcarnitines were measured in plasma and tissues of control turkeys, turkeys with an inbred spontaneous cardiomyopathy, and turkeys with furazolidone-induced cardiomyopathy. Heart failure was evident in both types of cardiomyopathy from decreased systemic blood pressure and cardiac dilatation compared to controls. Plasma free carnitine, short-chain acylcarnitine, and long-chain acylcarnitine were significantly elevated by 76 to 614% (p less than 0.01) in the two cardiomyopathy models compared to control. The highest carnitine levels were found in the most hypotensive turkeys. Liver free carnitine and short-chain acylcarnitine levels were also elevated by 45 to 537% (p less than 0.05) in both types of cardiomyopathy. Free carnitine was elevated by 126% in left ventricle and by 54% in skeletal muscle of the furazolidone-treated turkeys (p less than 0.05). We speculate that hepatic synthesis of carnitine may be increased in response to hypotension and progressive cardiac dysfunction in cardiomyopathic turkeys. Such an increase may be useful to promote beta-oxidation of fatty acids as a cardiac energy source.

Animals↗
PubMed2002

A specific force deficit exists in skeletal muscle after partial denervation.

Skeletal muscle demonstrates a specific force deficit after repair of injured peripheral nerves, microneurovascular muscle transfer, and normal aging. Because atrophy cannot account for deficits in specific force, other, unknown, mechanisms are responsible for the resulting muscle contractile dysfunction under these circumstances. We tested the hypothesis that a subpopulation of denervated fibers is partially or completely responsible for the specific force deficit after partial denervation of the rat extensor digitorum longus muscle (EDL). Adult Fisher rats underwent either sham exposure or partial transection of 80% of the cross-sectional area of the left deep peroneal nerve. After a 2-week recovery period, maximum isometric force (F(0)) was measured in situ and maximum specific force (sF(0)) was calculated for EDL from both control (n = 8) and partial denervation (n = 7) groups. Innervated fiber cross-sectional area (CSA(inn)) was measured directly from whole EDL cross sections after immunohistochemical labeling for neural cell adhesion molecule (NCAM), a marker of muscle fiber denervation. A corrected specific force value (sF(0-inn)) was calculated by normalizing F(0) to CSA(inn). Partial skeletal muscle denervation resulted in significant reductions in muscle mass, F(0), and sF(0). The percentage of muscle fibers expressing NCAM in the extrajunctional sarcolemma increased from 1.0 +/- 0.8% in control to 49 +/- 15% in partially denervated EDL muscles. A 62.7% deficit in EDL specific force was observed after partial denervation. Denervated muscle fibers accounted for 59.3% of this deficit, but sF(0-inn) still differed significantly between control and partially denervated muscles, with a 25.5% difference between groups. In partially denervated muscles, the specific force deficit is partially but not fully explained by a subpopulation of noncontractile, denervated fibers.

Animals↗
PubMed1989

Organ blood flow and cardiovascular effects of high-frequency oscillation versus conventional ventilation in dogs with right heart failure.

Mongrel dogs underwent a large (apex to pulmonary valve) right ventriculotomy to produce right ventricular dysfunction. Right ventriculotomy decreased cardiac output from 2.47 +/- 0.43 to 1.34 +/- 0.16 L/min (p less than .01), increased CVP from 3.7 +/- 1.5 to 8.3 +/- 2.4 mm Hg (p less than .01), and decreased mean systemic arterial pressure (MAP) from 143 +/- 16 to 121 +/- 21 mm Hg (p less than .01). There was no effect on mean pulmonary artery pressure (MPAP) or pulmonary artery occlusion pressure. After stabilization a randomized crossover controlled comparison of conventional mechanical ventilation (CMV) and high-frequency oscillation (HFO) was performed. FIO2, pH, PCO2, core temperature, and preload were held constant. Mean airway pressure (Paw) was 4.8 +/- 0.7 cm H2O on CMV vs. 3.5 +/- 1.0 cm H2O on HFO (p less than .05). There was no difference in PaO2. We found no statistically significant differences between the two modes of ventilation with respect to cardiac output, MAP, MPAP, systemic vascular resistance, and pulmonary vascular resistance. Blood flows to cerebral cortex, renal cortex, adrenal, hepatic artery, left ventricular myocardium, and skeletal muscle were not different when comparing CMV to HFO. Despite the ability to attain equivalent oxygenation and ventilation at lower Paw, HFO offers no hemodynamic advantage over CMV in the presence of right ventricular dysfunction.

Animals↗
PubMed2004

Electrical stimulation modifies spinal and cortical neural circuitry.

Sensory input shapes and refines motor performance. It also modulates, on both a short- and long-term basis, the neural circuitry underlying motor performance. Evidence suggests that electrical stimulation can be used to mimic these modulatory effects on neural circuitry, perhaps providing a tool to influence motor function in both able-bodied individuals and those with motor dysfunction caused by neurological injury.

Conditioning, Operant↗